Two leading scientists explain how circadian rhythms work and offer advice on lifestyle changes to improve your health

The History: Establishing the Fundamental Biology of Circadian Rhythms

The first thing to know about the study of circadian rhythms, also known as chronobiology, is that with few exceptions all organisms on the planet follow a circadian clock. From daffodils to sparrows, zebras to humans, everything under the sun follows the pattern of the sun. In 1729, French scientist Jean-Jacques d’Ortous de Mairan recorded the first observation of an endogenous, or built-in, circadian oscillation in the leaves of the plant Mimosa pudica. Even in total darkness, the plant continued its daily rhythms. This led to the conclusion that the plant was not simply relying on external cues, or zeitgebers, but also its own internal biological clock.

Two hundred years later, in the mid-20th century, the world of modern chronobiology blossomed. The field benefitted from contributions from a number of scientists, notably Colin Pittendrigh, the “father of the biological clock.” Pittendrigh studied the fruit fly Drosophila and shed light on how circadian rhythms entrain, or synchronize, to light-dark cycles.Jürgen Aschoff, a friend of Pittendrigh, also studied entrainment modeling, although they reached different conclusions about the manner in which entrainment occurs (parametric versus non-parametric, which you can read more about here and here). John Woodland Hastings and his lab also made important foundational discoveries about the role of light in circadian rhythms by studying luminescent dinoflagellates, a type of plankton. Erwin Bünning, who studied plant biology, also contributed foundational research in entrainment modeling, describing the relationship between organisms and light-dark cycles.

The next phase of chronobiology discovery began to articulate the specific molecular and genetic mechanisms of circadian rhythms. This came from the work of Ron Konopka and Seymour Benzer, who in the early 1970s aimed to identify specific genes that controlled the circadian rhythms in fruit flies. Konopka and Benzer are credited with discovering that a mutated gene, which they called period, disrupted the circadian clocks of the flies.This was the first discovered genetic determinant of behavioral rhythms. Jeffrey C. Hall, Michael Rosbash and Michael W. Young expanded Konopka and Benzer’s work by successfully showing how the period gene worked on the molecular level. Hall, Rosbash and Young — who were awarded the 2017 Nobel Prize in Physiology or Medicine — isolated the period gene, and then showed how the clock system worked on a molecular level.

Jumping from fruit flies to mice, Joseph Takahashi and his team discovered the mammalian clock gene in 1994 — appropriately dubbed clock — and characterized it as an “evolutionarily conserved feature of the circadian clock mechanism.” This gene discovery, along with the body of work by Hall, Rosbash, Young and the scientist Michael Greenberg, led to a watershed in chronobiological knowledge. Within a few years, the genes informing circadian rhythms in lower organisms were largely worked out.

Things have progressed steadily ever since, and, many of the findings in fruit flies and mice have shown remarkable conservation across species, meaning that there are analogous circadian genes that control the rhythms of more complex animals, including humans.

“The rising and the setting of the sun is still the primary influence on circadian rhythms, but other systems have steadily grown in scientific inquiry.”

The Current Research: Articulating the Role of Circadian Rhythms in Human Health and Disease

It’s important to note that the biology of circadian rhythms is incredibly complex — there are multiple scientific journals dedicated to the field of research — and as a result our understanding of the role biological clocks play in health is mostly a result of animal studies and human epidemiological studies. The experiments in lower organisms help articulate the molecular and genetic mechanisms at play, and then scientists can look at, say, how sleep disruption leads to increased incidence of type 2 diabetes, obesity, and cardiovascular disease.

The understanding of how circadian rhythms work has also expanded well beyond interaction with the light-dark cycle. “We have social cues, eating cues, and exercise or activity cues — it’s very diverse,” Yoo said. The rising and the setting of the sun is still the primary influence on circadian rhythms, but other systems have steadily grown in scientific inquiry. A large body of work has demonstrated that diet is a key extrinsic cue interacting with the intrinsic clocks, including Dr. Satchidananda Panda’s work on time-restricted feeding, or how the time of eating impacts health. (Endpoints covered Panda’s research at length, which you can read in The Complete Guide to the Science of Fasting.)

Overall, it is now clear that circadian rhythms perform a systemic role to orchestrate all aspects of physiology in our body, including vital organ functions, metabolism, immunity, cognition and more. Yoo’s research has been expanding the field, partnering with a chronic pain specialist to study the rhythms of pain in patients. Work is also being conducted on the role of the light-dark cycle and disruptions in circadian rhythms by jet lag on cancer growth. Such studies of circadian rhythms under normal and disease conditions are teaching us important new insights that can be harnessed for lifestyle changes (when to eat, how much to sleep) and for discovering drugs that can help modulate circadian rhythms. And there is plenty more research to be done in virtually all aspects of human health and disease.

Sleep

The most important thing you can do is keep your sleep and waking times consistentand get enough sleep — seven to nine hours is usually considered the right amount for adults. At this point the scientific research on not getting enough sleep or having disruptive sleep is conclusive: It has a negative impact on mood, focus, cognitive function, and ultimately is linked to chronic disease. What’s more some scientists suggest that circadian misalignment caused by social jet lag may be a widespread phenomenon in the western world contributing to health problems.

So when should you sleep? Typically the body begins to secrete melatonin around 9:00 p.m. This is the trigger to shut things down and go rest.Melatonin secretion ends around 7:30 a.m., and during the day, there is virtually no melatonin in the system. Working around that general window, adjusting for personal preferences based on your natural inclinations, is key for avoiding sleep fragmentation (waking throughout your sleep) and for maintaining optimal health.

Finally, light is a factor. The light-dark cycle no longer is the only influence on our system, since we now encounter artificial light constantly — but it still plays a primary role. Getting plenty of natural light early in the day and avoiding unnatural light (blue light from screens, for instance) in the evening will support circadian alignment.

A huge topic; one that I think will turn out to be extremely enlightening in the “mystery” of Asperger types…

Insomnia is a frequent finding in adults with Asperger syndrome

20 AS (Aspergers) without medication were compared with 10 healthy controls devoid of neuropsychiatric anamnesis. Clinical examination, blood test battery and head MRI excluded confounding somatic illnesses. Structured psychiatric interview for axis-I and axis-II disorders were given to both groups as well as Beck Depression Inventory and Wechsler adult intelligence scale, revised version.

Sleep quality was assessed with sleep questionnaire, sleep diary during 6 consecutive days and description of possible sleep problems by the participants own words was requested.

Results

compared with controls and with normative values of good sleep, AS adults had frequent insomnia. In sleep questionnaire 90% (18/20), in sleep diary 75% (15/20) and in free description 85% (17/20) displayed insomnia. There was a substantial psychiatric comorbidity with only 4 AS subject devoid of other axis-I or axis-II disorders besides AS. Also these persons displayed insomnia. It can be noted that the distribution of psychiatric diagnoses in AS subjects was virtually similar to that found among patients with chronic insomnia.

Conclusions

the neuropsychiatric deficits inherent of AS predispose both to insomnia and to anxiety and mood disorders. Therefore a careful assessment of sleep quality should be an integral part of the treatment plan in these individuals. Conversely, when assessing adults with chronic insomnia the possibility of autism spectrum disorders as one of the potential causes of this condition should be kept in mind.

Background

Asperger syndrome (AS) is a pervasive developmental disorder characterized by altered social interactions, restricted interests and repetitive and stereotyped behaviour as in autism but, contrary to the latter, should not show any significant delay in acquisition of language, psychomotor and cognitive skills [1]. According to epidemiological surveys AS is not uncommon, the prevalence being 0,35% in school-age children [2]. The prevalence of AS in adulthood is unknown but as AS is a continuous and lifelong disorder [1] it is reasonable to assume that it is not significantly lower than in childhood. Most studies on AS concentrate on childhood while there is scarcity of reports about the clinical and neurobiological characteristics of these individuals in adulthood.

Autism, AS and pervasive developmental disorder not otherwise specified (PDD-NOS) are commonly referred as “autistic spectrum disorders” [3]. In children with autism spectrum disorders the initiation and continuity of sleep are disturbed to a greater degree than in children with other developmental disorders [4]. More specifically, AS children reported in a sleep questionnaire study more dyssomnias, particularly difficulty in initiating and maintaining sleep, than age-matched controls [5].

DSM-IV defines insomnia as difficulty in initiating or maintaining sleep, or nonrestorative sleep, lasting at least one month and causing significant dysfunction during daytime [1]. It is further divided into primary and secondary type, depending on whether it is caused by mental disorder, substance abuse, other sleep disorder, a general medical condition.

AS is known to persist into adulthood [1,6], and it is probable that disorganization of sleep persists as well. Insomnia gives rise to emotional distress, daytime fatigue and loss of productivity [7] and should therefore be taken in consideration when planning rehabilitation of these individuals. As pointed out by Godbout et al 1998 [8], clinical observations suggest that AS subjects may present the same difficulties in initiation and maintaining of sleep as previously described in autism. We are not aware of studies concerning systematic assessment of insomnia in adults with AS.

Comorbid psychiatric disorders occur frequently in adults with AS [9,10]. They might cause changes in sleep profile and also by themselves lower sleep quality. There is no knowledge of impact of comorbid mood or anxiety disorder on sleep in AS patients.

Our hypothesis was that AS adults display a high grade of insomnia. Our aim was also to study psychiatric comorbidity and its impact on sleep quality in AS adults. The quality of sleep was evaluated using sleep questionnaire, sleep diary and a detailed description of possible sleep proble

The simplistic picture of the brain chopped into function-based pieces is wrong.

What visual perception tells us about mind and brain

Recent studies of visual perception have begun to reveal the connection between neuronal activity in the brain and conscious visual experience. Transcranial magnetic stimulation (TMS) of the human occipital lobe disrupts the normal perception of objects in ways suggesting that important aspects of visual perception are based on activity in early visual cortical areas. Recordings made with microelectrodes in animals suggest that the perception of the lightness and depth of visual surfaces develops through computations performed across multiple brain areas. Activity in earlier areas is more tightly correlated with the physical properties of objects whereas neurons in later areas respond in a manner more similar to visual perception.

Neuroscience research over the past 40 years has revealed that there are roughly 30 different visual areas in the primate brain, and that within these areas there are parallel streams of processing and distinct modules (1, 2). But how is neuronal activity in the different areas related to our conscious visual perception? How can our unitary visual experience be based on neural activity spread across distinct streams of processing in multiple brain areas? The answers to these questions have profound implications for our understanding of the relationship between mind and brain. Whereas earlier pioneering work focused on the delineation of visual areas in the brain and the neurons’ basic response properties, recent research attempts to expose the roles different areas play in perception and the extent to which there are hierarchies of visual computations.

Conscious visual experience is thought to be based on activity in visual areas of cerebral cortex, which receive input from the retina. Early cortical structures are organized topographically with regard to the visual world. This topography can be exploited to investigate the role of different visual areas in perception. For example, neuronal activity in visual cortex can be locally blocked by transcranial magnetic stimulation (TMS) and the effect on visual perception in the corresponding portion of the visual field can be assessed. Kamitani and Shimojo (3) briefly (40–80 ms) presented a large grid pattern to human observers, and after a delay of 80–170 ms, a single pulse of TMS was given to the occipital lobe. The TMS caused the observers to perceive a disk-shaped patch of homogeneous color in the visual field on the opposite side from the side of the brain given TMS (TMS-induced scotoma). When the visual stimulus was a grating composed of parallel lines rather than a rectilinear grid, the scotoma was distorted and appeared to be an ellipse with its short axis along the contours. This contour-dependent distortion appeared to reflect long-range interactions between neurons selectively responsive to similar orientations (4). Interestingly, the color perceived inside the scotoma was consistent with that of the background, which was presented after, not before, the grid or grating. Thus there appears to be filling-in backward in time to compensate for the local information blocked by the TMS. This is just one example from a large body of evidence suggesting that neural activity in early visual cortex is necessary for conscious experience of perception, and that neuronal connections and interactions at these levels are reflected in the content of perception.

Perception is actually much more complex than a simple topographical representation of the visual world. Its primary goal is to recover the features of external objects—a process termed unconscious inference by von Helmholtz (5, 6). What we see is actually more than what is imaged on the retina. For example, we perceive a three-dimensional world full of objects despite the fact that there is a simple two-dimensional image on each retina. In general, a particular retinal image may correspond to more than one object. For example, a circular patch of light on the retina could result from viewing a cylinder on end or a round ball from any perspective. Thus perception is inevitably an ambiguity-solving process. The perceptual system generally reaches the most plausible global interpretation of the retinal input by integrating local cues, as will be illustrated in the case of lightness perception next.

Black-and-white photographs make it clear that lightness alone conveys a great deal of information. The perception of lightness is far from a “pixel-by-pixel” representation of the light level on the retina. It is actually strongly influenced by context. Thus a gray piece of paper appears darker if it is surrounded by white than black (Fig. 1A). Although this deviation of lightness perception from physical reality might appear to be a case of a perceptual error, the spatial interactions underlying it may have an important perceptual purpose. We perceive surface lightness to be constant across surprisingly large changes in ambient illumination, a phenomenon called lightness constancy. In this example, as in other cases of perceptual constancy, the lighting and viewing conditions affect the retinal image of objects, and extensive spatial integration and normalization are performed to recover the constant attributes of the objects themselves.

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Figure 1

(A) Lightness induction. The small gray squares are identical but the one surrounded by black appears lighter than the square surrounded by white. (B) The response of a V1 neuron to a lightness induction stimulus. The receptive field of the neuron was centered on a uniform gray square. The luminance of the surrounding area was sinusoidally modulated. The cell’s response was synchronized to the surround modulation and correlated with the perceived lightness of the central patch, even though nothing changed within the receptive field. [Reproduced with permission from ref. 14 (Copyright 2001, National Academy of Sciences).]

At what point in the visual pathway from retina to the many cortical visual areas does the neural activity correlate with what we perceive? Do neurons in the retina, primary visual cortex (V1), and higher-level cortical areas contribute to perception equally? Or instead, does perception have a specific locus in the brain? To tackle these questions, Paradiso and coworkers (7, 8) assess the computations neurons perform in different visual areas and the extent to which neural responses correlate with either the physical or perceptual attributes of objects. They found that responses of neurons in the retina and visual thalamus depend on light level but they do not correlate with perceived lightness. These neurons appear to primarily encode information about the location of contours in the visual scene. Only in V1 were cells found that had responses correlated with perceived lightness (Fig. 1B). They also found that the average response of neurons in V1 is lightness constant. Thus the response of the neurons is relatively immune to changes in overall illumination—a property without which lightness would be of little behavioral value. These findings suggest that lightness information is first explicitly represented in visual cortex and that responses correlated with visual perception build in stages across multiple visual areas. The results combined with findings from other labs suggest that early visual processing focuses on the extraction of object contours, secondary processing stages are involved with the computation of lightness and later processing assigns color to objects.

As mentioned previously, the visual system has the difficult task of understanding a complex three-dimensional world from two-dimensional images on each retina. Images of objects at a distance other than at the fixation plane are projected to different relative positions on the two retinas. The relative position difference, called binocular disparity, provides an important cue for the brain’s computation of distance. However, there is much more to distance perception than the interpretation of binocular disparity. Consider a retinal image of a cross with crossed disparities (disparities that lead to perception of objects closer than the plane of fixation) added to the ends of the horizontal arms. Because of the disparities, the vertical edges of the horizontal arms can be unambiguously determined as being closer to the observer, whereas the depth of the horizontal edges remains ambiguous because there is no fixed disparity between the two retinal images. Two different three-dimensional objects are equally consistent with the retinal image: a horizontal bar in front of a vertical bar and a cross with horizontal arms bent forward. However, humans and monkeys almost always perceive the former (9, 10). The brain selects one interpretation among the possible surface structures.

The inferior temporal cortex (IT) represents the final stage of the visual pathway crucial for object recognition.Neurons in IT respond to shape, color, or texture. Recent studies show that many IT neurons also convey information on disparity (11) and disparity gradients (12). These findings lead to a new view that IT is involved in some aspects of depth perception. Indeed, the activity of some IT neurons encodes information on the relative depth order of surfaces rather than the local absolute disparity cues of the stimulus. For example, a population of IT neurons responds more strongly to a horizontal bar in front of a vertical bar than to a vertical bar in front of a horizontal bar, regardless of whether crossed or uncrossed disparities are added (Fig. 2). Other cells prefer different surface structures. This behavior of IT neurons is in contrast to that of disparity-selective V1 neurons that respond to local absolute disparity (13). Thus, the pathway from V1 to IT transforms information about binocular disparity that is based on the optics of the eye into a perceptually relevant representation of information about surface structure.

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Figure 2

(A) The relationship between disparity type and location and surface depth order perceived. Responses of IT neurons to these four stimuli were tested to determine whether their activity correlates with the perceived surface structure or with the type of disparity.

The studies of lightness perception and depth perception lead to a similar conclusion about the relationship between brain activity and conscious visual perception. Rather than being based on neural activity in one special area, visual perception involves progressive computations spread across multiple brain areas. Both early areas, as in the TMS study, and later areas, as in the study of area IT, are involved in perception. The visual system masterfully recovers information about the objects in our environment (or not! What about the importance of “attention to” selective environmental content – as is the case for inattentional blindness in NTs?) based partly on processes of integration and normalization and partly on hard-wired probabilities of what objects are most likely to result from particular retinal images.

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This post is about one type of “brain gadget”: a mini (minimal number of electrodes) wearable EEG with enormous appeal for narcissists who are also lazy!

If you are allergic to physics, go to discussion at bottom of post!

Muse Brain-sensing Headband

Meditation and yoga are terrific tools for reducing your stress levels and improving your concentration, but they can be tricky for a beginner to master. That’s where the new Muse headband comes in: It’s a headphone-sized piece of tech that fits around your head, measuring your brain’s electrical impulses toguide you toward nirvana.

How exactly does Muse do it? When you connect headphones to a smartphone running the Muse Calm app, you’ll be able to hear just how focused your brain is. As your mind slowly ceases to wander, you’ll hear increasingly soothing sounds like ocean waves or a gentle breeze.Remember all those New Age meditation tapes from the 70s?Each Muse session can be completed in just 3 minutes,allowing you to fit the tech in to even the busiest of lifestyles.

PRICE? JUST $299. Not for poor folk! Guess we’ll have to reach Nirvana the hard way!

Some physics involved…LOL

Just in case you may be entranced by the idea of all your neurons firing “in sync” as a state of Nirvana, think again…

Data, data, data. Wowie, zowie tech. But what does it mean?

More physics (unavoidable) LOL

Again, fascinating tech, but what does it mean for the person who utilizes the gadget?

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Let’s try a description from a pop-tech website:

Discovered in 1924 by a German Psychiatrist, Hans Berger, Electroencephalography technology, or EEG, works by measuring the difference in electrical field that is produced by neurotransmission in real time. In traditional EEG testing, rows of electrodes are placed on a person’s scalp with a wire that hooks them up to an amplifier that strengthens the waves that are picked up, and a computer which records all of the data.

The data is presented on a graph in real time as the electrodes are picking up the electrical field on the scalp. Scientists decode this databy analyzing the types of waves that are presented.(Actually a computer program does this) There are a total of five different wavelength patterns: Delta, Theta, Alpha, Beta, and Gamma (least to greatest in wavelength frequency).

Just as a traditional EEG cap places electrodes all across the skull, headbands like InteraXon’s Muse Brain Sensing Headband work by placing sensors along the forehead and behind the ears. Once the headset is paired with its application, the electrical impulses that are read by the sensors are immediately visualized in the app. Once the headset is paired with its application, the electrical impulses that are read by the sensors are immediately visualized in the app.

NOTE: The traditional EEG uses multiple sensors distributed over the skull surface: mini EEG headsets generally only place 2 active electrodes over the frontal lobes. What about the rest of the brain? Visual processing, etc.

These neural patterns that are picked up by the electrodes are then used by researchers to analyze cognitive behavior. A can of worms is opened here. For instance, in sleep research, researchers will look for delta waves to see how deep a patient is able to fall asleep. Likewise, they will look for higher frequency waves such as gamma or beta waves to check if the patient is still in REM sleep.

With its noninvasive method of use, this technology allows scientists and physicians to record when and where a particular activity has taken place in a subject’s brain. From these findings,they are then be able to interpret how the subject was feelingduring a particular conversation – were they bored and unresponsive? Engaged and thinking critically? Were they focused on the conversation or task without any interruptions?

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On the subject of interpretation:

Are these “interpretations” valid as true representations of what is going on in the brain or how it works globally? That is, psychological concepts / word concepts such as boredom, or the process of “thinking critically”, are subjective opinions on the part of humans doing the interpretation. (Just ask a variety of people what “critical thinking” entails! LOL)

How do researchers arrive at these “interpretations”(meanings), when “brain waves” are ranges of electrical frequencies (physical properties), but the “assumed meanings” (interpretations) of the brain waves are “embedded” (locked and loaded hypothesis) in the activities the subject is tasked with, such as viewing images of faces, contrived to “express” various emotions that have been pre-determined by the researchers?

These are entirely different categories(measurable, quantifiable electrical activity) vs. (subjective experience or opinion and abstract process)“connected by” sweeping conclusions that are drawn “as if by magic”.

Structuring “experiments” in order tofind confirmation of what you are seeking in your “locked and loaded hypothesis” is not valid. This is not to say that actual physical data collected is not valid: Whether or not someone is asleep or not is at least observable (by the common definition of sleep), but one will not find “bored” or other subjective states stamped on a part of the brain or mysteriously “hidden” in electrical activity.

This projection of “human concepts about brain functions” (which are invented by certain human brains) is evidence of magical thinking. The assignation of “brain chopped into parts” = actual organization of the brain is baseless.The leap to assigning “human language-generated concepts”(such as emotion words or other mental states such as boredom, which are identified by word descriptions, which are learned by individuals during socio-cultural indoctrination),to direct correlation with a “pan-human” brain design(that problem with “normal” again) reflects the imposition of anthropomorphism on the human brain itself!

Think about it!

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back to:

With the frontal cortex being the primary location for problem solving, judgement, and impulse control, it makes sense why the Muse Brain Sensing Headband has sensors that are placed along the forehead. (It’s also much cheaper and takes far less computing power)

While it may not be (is not) able to get an accurate read on the brain as a whole, it is able to track the activity of the frontal lobe, where our ability to control focus is located. Thus, this headband can strongly aid in training the frontal cortex to react more calmly to impulse and think through actions rationally with a more focused mindset. (Again, we have some “magical transformation taking place, which is in reality a subjective illusion due to the highly suggestible social human act of obedience to “authority” That is, the user, having spent $299.00 for this techy-looking, futuristic “headband” will dutiful believe that wearing the object 3 minutes a day, randomly, for maybe a week or two, will “work magic” on his or her brain, making the brain more “focused and intelligent” – and superior to their social competitors…

Consumer EEG systems did show a significantly more convenient and faster set up, which is optimal for their intended use in entertainment and self-help applications.However, their data quality was overall negatively affected by artifact susceptibility associated with the dry electrode. As expected, the data quality was particularly diminished during EO. The lack of impedance testing capability and application to the frontal region, which is particularly prone to eye blinks and muscle movement with eye opening also likely contributed to this relative artifact. Additionally, the assessment performed by consumer EEG systems is, by their nature, limited and confined to the only anatomical brain region covered by the few channels, precluding multi-networks evaluations.

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I have spent some serious time trying to understand the roots of American psychological juvenalization-infantalization, because it “happened” during my lifetime, which is not that many years, and yet neotenic trends are driving contemporary behavior and failure.

“Neoteny” (I use neoteny here not scientifically, but as the tag for juvenile-infantile behavior in what ought to be proto or full adults) is a process that has been veiled by political upheaval from the 1960s until the present day; no one has talked seriously about the phenomenon until recently, but psychological childishness is rampant in our behavior and beliefs. Economically it’s a bonanza promoted by corporations and exploited by the market. Politicians pander to juvenile insecurity and need for attention.

My generation discovered that the “world” (having just been saved from Fascism by our parents) was still at war – the Cold War – about the time we popped out of baby-narcissism and into elementary consciousness at school. We were not spared reality by parents and teachers: our tender and innocent childhood years were spent waiting for the worst death imaginable to fall from the sky, without warning, giving us but a few minutes to cower under our school desks and imagine what was coming – incineration of everything we knew; parents, friends, our school and town, the United States, and perhaps most of the life on earth. Videos, posters and TV programs made annihilation both present and inevitable.

Despite the propaganda of American stability and supremacy, there really was nothing solid under our feet.

Existential anxiety? Long term effects? Denial would soon blossom into decades of sex, drugs and rock n roll.

Over the intervening years deep changes have occurred in the American mind. We live today in a scary state of incompetence with politicians vowing to resurrect “greatness.” That’s hard to do when a nation of 300 million people no longer comprehends what simple adult behavior requires: humility, sacrifice, personal integrity. What bizarre and forgotten qualities these Old-fashioned words represent.

At one point I began to think that perhaps Soviet agents had managed to put “dumb pills” in municipal water supplies, but now I think I have identified the true cause of diminished American mental abilities: A massive influx of neotenic toys and images from Japan during the 1960s.

NOTE: This so-called therapy is not approved by the FDA to “treat” Autism, and yet it is being promoted for treating ASD / Asperger types.

Keyword: ka-ching

From the website: About Us

The Center for Integrative & Innovative Therapies (The CIIT Center) is all about the intimate relationships among the patient, doctors, and therapists, all working together under one roof! What sets The CIIT Center apart from other facilities is that our doctors and therapists look beyond the obvious symptoms that our patients are experiencing and they use innovative diagnostic tests and integrative therapies to treat the core, underlying health conditions and not just the symptoms. That’s when your personalized treatment program begins….

The CIIT Center believes in Integrative Medicine as the core to our treatment protocol and we treat the patient as a whole person, including all aspects of their lifestyle. We treat each patient with an integrative approach that includes a customized treatment plan of various therapies. Our healthcare professionals work in unison to develop an individualized health plan all in one facility.

We’ll find mysterious imaginary things wrong with you; trust us. We have our own “doctors” who will make sure you are diagnosed with “something” that we can turn into $$$$$$$$$$$$$$$ .

What is TMS?

Transcranial Magnetic Stimulation (TMS) is a drug-free, painless, non-invasive therapy that uses magnetic pulses to stimulate your brain. It is FDA approved for patients who are suffering from Depression that have had poor results from antidepressants.If you don’t have depression and/or are not taking anti-depressants, this so-called therapy is not approved by the FDA for you. Of course, these nice people will “find someone” (their doctor) who will diagnose your non-existent depression.

How does TMS work?

TMS works by sending magnetic pulses into your brain. It is non-invasive and doesn’t involve any drugs or sedatives. During Depression, there is an area of your brain (Dorsal lateral prefrontal cortex, a.k.a. DLPFC) that is electrically under-active. By stimulating the nerves of the DLPFC, one may experience improvements in both mood and Depression symptoms. These improvements have the potential to lift one out of Depression and decrease one’s reliance on antidepressants or other mood-related medications. How magical! How non-committal. How simple! Of course, if it doesn’t improve your complaint, we still get paid!

Note how quickly this topic pops up!Is TMS covered by Insurance?

You are diagnosed with Major Depressive Disorder (no problem; our staff doctors can do that!) AND

You’ve tried at least 2 different antidepressants along with psychotherapy and haven’t had success (Since the failure rate of these two “treatments” is very high (and improvement unverifiable) almost anyone who has “tried” these, will qualify.

Medicare will cover TMS Therapy if you meet the above criteria.

Other insurance companies can be very specific when covering TMS Therapy. If our doctors think you are a potential candidate for TMS,we will contact your insurance company(apply pressure, and negotiate a deal?) to verify that they will cover your TMS treatment. Coverage varies per insurance company and it can take some time (days to weeks) to receive approval. We suggest making an appointment as soon as possible so that the process can get a head start. Call us at xxx-xxx-xxxx to make an appointment or learn more about TMS.

We also offer TMS Therapy for other conditions such as Anxiety, Traumatic Brain Injury (TBI), Concussions, Obsessive Compulsive Disorder (OCD), and Post Traumatic Stress Disorder (PTSD). However,treatment for conditions other than Depression is considered off-label and insurance will normally not cover the cost. As a result, payment will likely be out-of-pocket. However, we do offer payment plans with discounted rates. Please call us at xxx-xxx-xxxx to discuss or to make an appointment with a doctor.

How long does TMS Therapy last?

Your first session of TMS will last about 60 minutes: 20-30 minutes of preparation and 20-30 minutes of actual treatment. Subsequent sessions will be streamlined and should normally last 20 minutes, though the length of your session may vary depending on the doctor’s orders and the conditions we’re treating.

In order for the treatment to be effective, we ask patients to be available for 5 days a week (3 days minimum) for at least 6 weeks. When streamlined, each session usually lasts only 20-25 minutes per day. A full TMS course typically consists of 36 treatments, with the final 6 treatments spaced out. COST?

What can I expect during TMS?

Your first session of TMS will involve a technician taking measurements for your personal TMS cap and asking questions pertaining to your health. After the measurements are done, the technician will take a motor threshold (MT). The MT is used to determine the intensity of your treatment, based on an involuntary motor reflex. After preparations are done, you will sit in an adjustable chair and be able to watch TV during treatment. The coil will then be placed against your head and treatment will begin. The machine will provide a “heads-up” beep before each pulse. Some patients report that the pulses feel like someone “tapping” on your head rapidly while others report involuntary facial twitches. The treatment will continue to run for its prescribed time, after which the technician will remove the coil and your cap and you will be free to continue your day.

Well! Sit in a comfy chair; watch TV; wear a little cap; how fun! Think of the endless blah, blah, blah social mileage you’ll get out of this adventure! It’s just like going to the salon-spa to get your hair styled. In fact, just think of it as a “styling treatment” for your brain!

Will these supposedly high-tech treatments someday join the catalogue of electro-magnetic gadget quackery?